Marcia Gracindo Silva, Camila Guerra Martinez, Joao Paulo Cavalcanti de Albuquerque, André Luiz Gouvêa, Monica Maria Freire, Leidiane Caroline Lauthartte, Julio Mignaco, Wanderley Rodrigues Bastos, Elisabete Cesar de Mattos, Antonio Galina, Eleonora Kurtenbach
{"title":"线粒体功能障碍在甲基汞引起的心脏毒性中发挥着重要作用","authors":"Marcia Gracindo Silva, Camila Guerra Martinez, Joao Paulo Cavalcanti de Albuquerque, André Luiz Gouvêa, Monica Maria Freire, Leidiane Caroline Lauthartte, Julio Mignaco, Wanderley Rodrigues Bastos, Elisabete Cesar de Mattos, Antonio Galina, Eleonora Kurtenbach","doi":"10.3390/toxics12100712","DOIUrl":null,"url":null,"abstract":"<p><p>The effects of methylmercury (MeHg) on exposed populations are a public health problem. In contrast to widely studied neurological damage, few cardiovascular changes have been described. Our group evaluated the cardiotoxicity of a cumulative dose of 70 mg.kg<sup>-1</sup> fractioned over a 14-day exposure period in mice (MeHg70 group). The effects of MeHg on proteins relevant to cardiac mitochondrial function were also investigated. The results obtained showed a reduction in oxygen consumption in the two settings. In cardiac tissue samples in oxygraphy studies, this reduction was related to a lower efficiency of complexes II and V, which belong to the oxidative phosphorylation system. In vivo, mice in the MeHg70 group presented lower oxygen consumption and running tolerance, as shown by ergometric analyses. Cardiac stress was evident in the MeHg70 group, as indicated by a marked increase in the level of the mRNA encoding atrial natriuretic peptide. Electrocardiogram studies revealed a lower heart rate at rest in the animals from the MeHg70 group, as well as prolonged left ventricular depolarisation and repolarisation. Through echocardiographic analysis, reductions in the left ventricular ejection fraction and left ventricular wall thickness of approximately 10% and 20%, respectively, were detected. These results indicate that the oral intake of MeHg can decrease cardiac function and oxidative metabolism. This finding highlights the importance of monitoring MeHg levels in humans and animals in contaminated areas, as well as periodically carrying out cardiac function tests.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 10","pages":""},"PeriodicalIF":3.9000,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511492/pdf/","citationCount":"0","resultStr":"{\"title\":\"Mitochondrial Dysfunction Plays a Relevant Role in Heart Toxicity Caused by MeHg.\",\"authors\":\"Marcia Gracindo Silva, Camila Guerra Martinez, Joao Paulo Cavalcanti de Albuquerque, André Luiz Gouvêa, Monica Maria Freire, Leidiane Caroline Lauthartte, Julio Mignaco, Wanderley Rodrigues Bastos, Elisabete Cesar de Mattos, Antonio Galina, Eleonora Kurtenbach\",\"doi\":\"10.3390/toxics12100712\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The effects of methylmercury (MeHg) on exposed populations are a public health problem. In contrast to widely studied neurological damage, few cardiovascular changes have been described. Our group evaluated the cardiotoxicity of a cumulative dose of 70 mg.kg<sup>-1</sup> fractioned over a 14-day exposure period in mice (MeHg70 group). The effects of MeHg on proteins relevant to cardiac mitochondrial function were also investigated. The results obtained showed a reduction in oxygen consumption in the two settings. In cardiac tissue samples in oxygraphy studies, this reduction was related to a lower efficiency of complexes II and V, which belong to the oxidative phosphorylation system. In vivo, mice in the MeHg70 group presented lower oxygen consumption and running tolerance, as shown by ergometric analyses. Cardiac stress was evident in the MeHg70 group, as indicated by a marked increase in the level of the mRNA encoding atrial natriuretic peptide. Electrocardiogram studies revealed a lower heart rate at rest in the animals from the MeHg70 group, as well as prolonged left ventricular depolarisation and repolarisation. Through echocardiographic analysis, reductions in the left ventricular ejection fraction and left ventricular wall thickness of approximately 10% and 20%, respectively, were detected. These results indicate that the oral intake of MeHg can decrease cardiac function and oxidative metabolism. This finding highlights the importance of monitoring MeHg levels in humans and animals in contaminated areas, as well as periodically carrying out cardiac function tests.</p>\",\"PeriodicalId\":23195,\"journal\":{\"name\":\"Toxics\",\"volume\":\"12 10\",\"pages\":\"\"},\"PeriodicalIF\":3.9000,\"publicationDate\":\"2024-09-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511492/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxics\",\"FirstCategoryId\":\"93\",\"ListUrlMain\":\"https://doi.org/10.3390/toxics12100712\",\"RegionNum\":3,\"RegionCategory\":\"环境科学与生态学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENVIRONMENTAL SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxics","FirstCategoryId":"93","ListUrlMain":"https://doi.org/10.3390/toxics12100712","RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
引用次数: 0
摘要
甲基汞(MeHg)对暴露人群的影响是一个公共健康问题。与广泛研究的神经系统损害不同,很少有关于心血管变化的描述。我们的研究小组评估了小鼠(甲基汞 70 组)在 14 天暴露期中 70 毫克/千克-1 的累积剂量对心血管的毒性。我们还研究了甲基汞对与心脏线粒体功能相关的蛋白质的影响。结果表明,在这两种情况下,耗氧量都有所下降。在氧饱和度研究的心脏组织样本中,这种降低与属于氧化磷酸化系统的复合体 II 和 V 的效率降低有关。在体内,MeHg70 组小鼠的耗氧量和耐跑能力较低,这一点已通过测力分析表明。甲基汞 70 组小鼠的心脏压力明显增加,这表现在编码心房利钠肽的 mRNA 水平显著升高。心电图研究显示,MeHg70 组动物静息时心率较低,左心室去极化和复极化时间延长。通过超声心动图分析,发现左心室射血分数和左心室壁厚度分别降低了约 10%和 20%。这些结果表明,口服甲基汞会降低心脏功能和氧化代谢。这一发现强调了监测污染区人类和动物体内甲基汞水平以及定期进行心脏功能测试的重要性。
Mitochondrial Dysfunction Plays a Relevant Role in Heart Toxicity Caused by MeHg.
The effects of methylmercury (MeHg) on exposed populations are a public health problem. In contrast to widely studied neurological damage, few cardiovascular changes have been described. Our group evaluated the cardiotoxicity of a cumulative dose of 70 mg.kg-1 fractioned over a 14-day exposure period in mice (MeHg70 group). The effects of MeHg on proteins relevant to cardiac mitochondrial function were also investigated. The results obtained showed a reduction in oxygen consumption in the two settings. In cardiac tissue samples in oxygraphy studies, this reduction was related to a lower efficiency of complexes II and V, which belong to the oxidative phosphorylation system. In vivo, mice in the MeHg70 group presented lower oxygen consumption and running tolerance, as shown by ergometric analyses. Cardiac stress was evident in the MeHg70 group, as indicated by a marked increase in the level of the mRNA encoding atrial natriuretic peptide. Electrocardiogram studies revealed a lower heart rate at rest in the animals from the MeHg70 group, as well as prolonged left ventricular depolarisation and repolarisation. Through echocardiographic analysis, reductions in the left ventricular ejection fraction and left ventricular wall thickness of approximately 10% and 20%, respectively, were detected. These results indicate that the oral intake of MeHg can decrease cardiac function and oxidative metabolism. This finding highlights the importance of monitoring MeHg levels in humans and animals in contaminated areas, as well as periodically carrying out cardiac function tests.
ToxicsChemical Engineering-Chemical Health and Safety
CiteScore
4.50
自引率
10.90%
发文量
681
审稿时长
6 weeks
期刊介绍:
The Journal accepts papers describing work that furthers our understanding of the exposure, effects, and risks of chemicals and materials in humans and the natural environment as well as approaches to assess and/or manage the toxicological and ecotoxicological risks of chemicals and materials. The journal covers a wide range of toxic substances, including metals, pesticides, pharmaceuticals, biocides, nanomaterials, and polymers such as micro- and mesoplastics. Toxics accepts papers covering:
The occurrence, transport, and fate of chemicals and materials in different systems (e.g., food, air, water, soil);
Exposure of humans and the environment to toxic chemicals and materials as well as modelling and experimental approaches for characterizing the exposure in, e.g., water, air, soil, food, and consumer products;
Uptake, metabolism, and effects of chemicals and materials in a wide range of systems including in-vitro toxicological assays, aquatic and terrestrial organisms and ecosystems, model mammalian systems, and humans;
Approaches to assess the risks of chemicals and materials to humans and the environment;
Methodologies to eliminate or reduce the exposure of humans and the environment to toxic chemicals and materials.